Fetal X-Ray Exposure Interferes with Memory in Adulthood

Disrupted Cortical Development in a Primate Model of Schizophrenia

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Philadelphia, 5 July, 2010 - Learning and memory impairments are important contributors to the disability associated with schizophrenia. These functional impairments emerge long before the onset of other symptoms associated with schizophrenia, suggesting that they are a consequence of a disturbance in brain development.

In order to investigate the impact of early life disturbances in brain development upon learning and memory, researchers at the Yale University School of Medicine conducted a study that required a remarkable degree of commitment and planning. They exposed fetal monkeys to x-rays and then examined their behavior when they were adults, approximately 5 years later.

They found that irradiated adult monkeys exhibited a profound deficit in working memory ability compared to adult monkeys that had not been exposed to x-rays. Notably, these same irradiated monkeys had not shown any working memory impairment when tested as juveniles (1 - 2½ years old). These findings suggest that this relatively mild insult to the developing brain early in gestation, even before cortical neurons are generated, produced profound cognitive dysfunction that emerged only with maturation to adulthood.

It is important to note that this study evaluated the effects of exposure to x-rays at a much higher level than would be associated with the typical x-ray, so the authors do not suggest that typical clinical x-ray exposures cause schizophrenia in humans.

However, notes Dr. Selemon, “this study reaffirms the importance of the early gestational period as a critical window of vulnerability to environmental factors that may have adverse effects on brain development and insidious consequences for brain function.”

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Notes to Editors
The article is “Fetal Irradiation Interferes with Adult Cognition in the Nonhuman Primate” by Harriet R. Friedman and Lynn D. Selemon. The authors are affiliated with the Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut. The article appears in Biological Psychiatry, Volume 68, Issue 1 (July 1, 2010), published by Elsevier.

The authors’ disclosures of financial and conflicts of interests are available in the article.

Full text of the article mentioned above is available upon request. Contact Maureen Hunter at m.hunter@elsevier.com to obtain a copy or to schedule an interview.

About Biological Psychiatry
This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Commentaries, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly.

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